Evidence map›Paper›PMID 25862682›Full record

ArticleThe Journal of antimicrobial chemotherapy2015

Multiple mutations and increased RNA expression in tetracycline-resistant Streptococcus pneumoniae as determined by genome-wide DNA and mRNA sequencing.

Andréanne Lupien, Hélène Gingras, Michel G Bergeron, Philippe Leprohon, Marc Ouellette

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of antimicrobial chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Evolution, Mechanisms, and Therapeutic Implications of Mobile Tetracycline Destructases.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
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  5. Serotype distribution and antibiogram ofMicrobiology spectrum · 2023
    Article
  6. Article
  7. Preventive effect ofFrontiers in cellular and infection microbiology · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Andréanne LupienCentre de recherche en Infectiologie du Centre de recherche du CHU de Québec and Département de Microbiologie, Infectiologie et Immunologie, Faculté de Médecine, Université Laval, Québec, QC, Canada.
Hélène GingrasCentre de recherche en Infectiologie du Centre de recherche du CHU de Québec and Département de Microbiologie, Infectiologie et Immunologie, Faculté de Médecine, Université Laval, Québec, QC, Canada.
Michel G BergeronCentre de recherche en Infectiologie du Centre de recherche du CHU de Québec and Département de Microbiologie, Infectiologie et Immunologie, Faculté de Médecine, Université Laval, Québec, QC, Canada.
Philippe LeprohonCentre de recherche en Infectiologie du Centre de recherche du CHU de Québec and Département de Microbiologie, Infectiologie et Immunologie, Faculté de Médecine, Université Laval, Québec, QC, Canada.
Marc OuelletteCentre de recherche en Infectiologie du Centre de recherche du CHU de Québec and Département de Microbiologie, Infectiologie et Immunologie, Faculté de Médecine, Université Laval, Québec, QC, Canada marc.ouellette@crchul.ulaval.ca.
Centre hospitalier de l'Université Laval · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

objectivesThe objective of this study was to characterize chromosomal mutations associated with resistance to tetracycline in Streptococcus pneumoniae.

methodsChronological appearance of mutations in two S. pneumoniae R6 mutants (R6M1TC-5 and R6M2TC-4) selected for resistance to tetracycline was determined by next-generation sequencing. A role for the mutations identified was confirmed by reconstructing resistance to tetracycline in a S. pneumoniae R6 WT background. RNA sequencing was performed on R6M1TC-5 and R6M2TC-4 and the relative expression of genes was reported according to R6. Differentially expressed genes were classified according to their ontology.

resultsWGS of R6M1TC-5 and R6M2TC-4 revealed mutations in the gene rpsJ coding for the ribosomal protein S10 and in the promoter region and coding sequences of the ABC genes patA and patB. These cells were cross-resistant to ciprofloxacin. Resistance reconstruction confirmed a role in resistance for the mutations in rpsJ and patA. Overexpression of the ABC transporter PatA/PatB or mutations in the coding sequence of patA contributed to resistance to tetracycline, ciprofloxacin and ethidium bromide, and was associated with a decreased accumulation of [(3)H]tetracycline. Comparative transcriptome profiling of the resistant mutants further revealed that, in addition to the overexpression of patA and patB, several genes of the thiamine biosynthesis and salvage pathway were increased in the two mutants, but also in clinical isolates resistant to tetracycline. This overexpression most likely contributes to the tetracycline resistance phenotype.

conclusionsThe combination of genomic and transcriptomic analysis coupled to functional studies has allowed the discovery of novel tetracycline resistance mutations in S. pneumoniae.

Indexed as

MutationTetracycline ResistanceDNA, BacterialGenome, BacterialMolecular Sequence DataRNA, BacterialRNA, MessengerSelection, GeneticSequence Analysis, DNAStreptococcus pneumoniaeTetracyclineDNA, BacterialRNA, BacterialRNA, MessengerTetracyclineABC transportersgenomicRNA-seqrpsJS. pneumoniaethiamine

Identifiers

PMID25862682
PMCPMC4472328
OpenAlexW2121550854

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.